Sudden infant death syndrome (SIDS) has a ten-fold likelihood of occurring in a low birth weight infant. Sleep appears to be a necessary factor for the development of SIDS. It is known from studies on adults that respiratory chemosensitivity to carbon dioxide is depressed during sleep. Whether or not a similar depression of chemosensitivity takes place during sleep in infancy is not known. Studies of respiratory chemosensitivity to carbon dioxide in low birth weight infants suggest that the appearance of chemosensitivity is related to neurological maturation. When compared to term infants, low birth weight infants exhibit reduced chemosensitivity until they reach a similar post- conceptional age. The apnea of prematurity appears to be a clinical manifestation of thi reduction in chemosensitivity. It has been noted that infants with apnea appear to be asleep. Thus apnea of prematurity not only occurss in a froup of infants later at high risk from SIDS, but may in fact be a model of SIDS as well. It is proposed to administer 2.5% CO2, 5% CO2, and room air to sleeping infants while monitoring their minute volume, heart rate, EEG, EMG, and EOG activity. The slope of the line minute volume/Pco2 will be an index of CO2 sensitivity. It is also proposed to monitor low birth weight premature infants to determine if apnea occurs during sleep, as determined by EEG and EMG tracings. Finally, it is proposed to determine the maturation of response to CO2 by following infants up to 100 weeks post-conception. (approximately 1 year of age) with the same studies as performed in early infancy.